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PubMed1997

[Thoracic surgery and liver dysfunction].

Lung resection results in loss of lung parenchyma including residual healthy lung tissue and in reduction in pulmonary vascular bed. A decrease in residual pulmonary vascular bed after lung resection causes an increase in right heart afterload, and in some patients, it would be associated with an increase in right heart preload and consequent the changes in hepatic circulation which would lead to liver damage. Preceding thoracotomy, unilateral pulmonary arterial occlusion test (UPAO) was performed to simulate the hemodynamic changes after lung resection to evaluate the increase in right heart preload after surgery. Patients with the decreases in cardiac index or PaO2 during UPAO showed a higher levels of GPT during postoperative period when compared with those with the increase in either parameters. In a surgical treatment for empyema, bronchiectasis, or other infectious lung diseases, bronchial angiography (BAG) and also bronchial arterial embolization (BAE) were useful methods to prevent from exceeding bleeding during thoracotomy, which is one of the risk factors to cause liver damage after surgery. These results suggest that, in the field of thoracic surgery, the preoperative assessment of the hemodynamic changes caused by lung resection and the preoperative attempt to prevent from bleeding during thoracotomy are both important to protect from liver damage caused by surgical stress.

Empyema↗
PubMed1996

Iron overload and liver dysfunction after allogeneic or autologous bone marrow transplantation.

Patients who require a bone marrow transplant (BMT) for leukaemia, lymphoma or other haematological disorders receive large quantities of blood products, including red cell concentrates, during the transplant period. Many receive red cell transfusions as part of treatment prior to BMT, adding to the potential iron load. However, organ dysfunction as a consequence of the transfused iron load would be surprising given the amounts of iron transfused. We studied 76 survivors of allogeneic and autologous BMT who were at least 1 year post-transplant and found that the majority (88%) had raised ferritins. Impaired liver function was common in these patients and in half was unexplained by viral hepatitis, veno-occlusive disease or graft-versus-host disease (GVHD), suggesting that iron overload may be an important contributing factor to liver disease in the stable post-transplant setting. This view is supported by the observation of improving liver function tests in 10 patients after a trial of venesection therapy.

Adolescent↗
PubMed1985

The use of different doses of vecuronium in patients with liver dysfunction.

The clinical neuromuscular effects of two doses of vecuronium (0.15 mg kg-1 and 0.2 mg kg-1) were investigated in 20 healthy patients and 20 patients with cirrhosis, and compared with previous work in which vecuronium 0.1 mg kg-1 was given under identical conditions of anaesthesia and monitoring. Ten healthy patients received vecuronium 0.15 mg kg-1 and 10 received 0.2 mg kg-1. Similarly, 10 patients with cirrhosis received vecuronium 0.15 mg kg-1 and 10 received 0.2 mg kg-1. Vecuronium 0.1 mg kg-1 has previously been shown to have a somewhat shorter duration of action in cirrhotic as opposed to healthy patients. In this study, vecuronium 0.15 mg kg-1 was found to have a similar duration of action in both groups, and vecuronium 0.2 mg kg-1 had a significantly longer action in the cirrhotic group. It is suggested that vecuronium should be used with caution in patients with hepatic dysfunction and that, in such patients, monitoring of neuromuscular function is desirable.

Adult↗
PubMed1994

Pharmacokinetic behavior of cyclosporine A in liver dysfunction.

The pharmacokinetic behavior of cyclosporine A (CyA), known as a potential immunosuppressive agent to prevent graft rejection in transplantation, was studied in patients with acute hepatitis and primary biliary cirrhosis (PBC). The ratios of blood concentration of total CyA (CyA and its metabolites), CyA, and CyA metabolites to dose/kg body weight, (t-CyA/dose, CyA/dose, and CyA-Met/dose, respectively) were significantly higher in patients with hepatitis than those in renal transplantation. In PBC patients these ratios showed a tendency to be smaller than those in renal transplantation, but were not significant. The ratio of CyA-Met/CyA was higher in the patients with hepatitis and PBC than that in renal transplantation. It was highest in the patients with PBC. The ratio of CyA-Met/CyA was significantly increased with a decrease of liver functions evaluated by serum glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and total serum bilirubin (t-Bil). These results indicate that hepatic function affects the pharmacokinetic behavior of CyA and the increased ratio of CyA-Met/dose could be caused by a possible increased efflux of metabolites into the blood circulation due to impaired bile excretion. These results also indicate the importance of therapeutic drug monitoring (TDM) in the use of CyA with patients with hepatic dysfunction.

Acute Disease↗
PubMed1987

Captopril-induced liver dysfunction.

We have described a patient with captopril-induced cholestatic jaundice. Captopril was confirmed as the causative agent, because jaundice occurred after administration of captopril and resolved quickly after administration was stopped.

Captopril↗
PubMed1990

Subclinical liver dysfunction in one-month-old infants with a low activity of vitamin K dependent coagulant factors assessed by normotest.

To clarify features of late vitamin K deficiency hemorrhagic disease in Japanese infants, seventeen of 1,687 infants screened by normotests were examined for signs and symptoms suggesting hepatobiliary diseases. Clinical observations disclosed findings suggesting hepatobiliary diseases in 7 of the 17 selected infants with normotest values of less than 40%, and 11 infants had abnormal results in one or more liver function tests. Taken together, 14 of the 17 infants had findings suggesting hepatobiliary diseases. Upon vitamin K supplementation normotest values improved in various degrees in all infants, whether or not they had signs or symptoms of hepatobiliary diseases. Late vitamin K deficiency hemorrhagic disease of infancy may be related to subclinical hepatobiliary diseases.

Female↗
PubMed2002

Bile system morphogenesis defects and liver dysfunction upon targeted deletion of HNF1beta.

The inactivation of the Hnf1beta gene identified an essential role in epithelial differentiation of the visceral endoderm and resulted in early embryonic death. In the present study, we have specifically inactivated this gene in hepatocytes and bile duct cells using the Cre/loxP system. Mutant animals exhibited severe jaundice caused by abnormalities of the gallbladder and intrahepatic bile ducts (IHBD). The paucity of small IHBD was linked to a failure in the organization of duct structures during liver organogenesis, suggesting an essential function of Hnf1b in bile duct morphogenesis. Mutant mice also lacked interlobular arteries. As HNF1beta is not expressed in these cells, it further emphasizes the link between arterial and biliary formation. Hepatocyte metabolism was also affected and we identified hepatocyte-specific HNF1beta target genes involved in bile acids sensing and in fatty acid oxidation.

Acyl-CoA Dehydrogenase, Long-Chain↗